RNA Sequencing Analysis of the epididymal adipose tissue from Normal Chow, HFD Control and SZ-A-treated HFD mice
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ABSTRACT:
ORGANISM(S): Mus musculus
PROVIDER: GSE214618 | GEO | 2022/11/20
REPOSITORIES: GEO
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Project description:Ramulus Mori (Sangzhi) alkaloids (SZ-A) alleviates nonalcoholic fatty liver disease in mice. This study compares transcriptome profiling (RNA-seq) in the liver of normal chow, high-fat diet (HFD) control and SZ-A-treated HFD mice to verify the regulatory mechanisms of SZ-A. These results demonstrated that SZ-A regulates lipid metabolism and metabolic stress-induced inflammation and fibrosis.
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Project description:RNA Sequencing Analysis of liver from Normal Chow, HFD Control and SZ-A-treated HFD mice
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Project description:The novel Traditional Chinese Medicine Ramulus Mori (Sangzhi) alkaloid tablets (SZ-A) are approved by The China National Medical Products Administration for the treatment of type 2 diabetes mellitus (T2DM). However, the extensive pharmacological characteristics and the underlying mechanism are unknown. This study investigated the mechanisms by which SZ-A ameliorates glucose metabolism in KKAy mice, an animal model of T2DM. Diabetic KKAy mice were treated intragastrically with SZ-A once daily for 8 weeks, after which glucose levels, lipid metabolism, gut microbiome, systemic inflammatory factors, luminal concentrations of short-chain fatty acids (fecal samples), and ileal proteomic changes were evaluated. The ileum tissues were collected, and the effects of SZ-A on pathological inflammatory damage were evaluated by hematoxylin and eosin staining, immunofluorescence, and immunohistochemistry. The mRNA and protein expression levels of various inflammatory markers, including monocyte chemoattractant protein-1 and phosphorylated nuclear factor kappa B p65, were detected in the ileum tissues. SZ-A improved glucose metabolism with enhanced insulin response and elevated glucagon-like peptide 1 (GLP-1) during the glucose tolerance test in diabetic KKAy mice. Gut microbiota analysis demonstrated that SZ-A administration elevated the abundance of Bacteroidaceae and Verrucomicrobia, reduced the levels of Rikenellaceae and Desulfovibrionaceae; and increased the concentrations of fecal acetic and propionic acids compared to the diabetic model group. Additionally, SZ-A markedly improved ileal inflammatory injury and pro-inflammatory macrophage infiltration and improved intestinal mucosal barrier function in diabetic KKAy mice. SZ-A also attenuated the levels of circulating endotoxin, pro-inflammatory cytokines, and chemokines in the mice sera. Collectively, SZ-A ameliorated the overall metabolic profile including glucose and lipid metabolism in KKAy mice, which may be associated with an improvement in GLP-1 and insulin secretion, at least in part by modulating the gut microbiome and relieving the degree of ileal and systemic inflammation.
2021-09-10 | PXD024241 | Pride
Project description:Purpose: Aim of the study is to identify changes in hepatic gene expression induced by either a 40kcal% coconut oil rich high fat diet (HFD), a 40kcal% soybean oil plus coconut oil high fat diet (SO-HFD) or a low fat vivarium chow diet (Viv). Methods: Livers from mice that had been fed one of the above mentioned diets for 35 weeks, were used to make cDNA libraries that were then sent for deep sequencing, using the Illumina TruSeq RNA. Result: Many genes involved in metabolism, lipid binding, transport and storage and many Cyp genes are dysregulated in the two high fat diets as compared to Viv HFDs in SO-HFD mice. Comparing the two HFDs shows more metabolism and disease related genes dysregulated in SO-HFD vs HFD. Conclusion: A diet high in soybean oil may be more detrimental to metabolic health than a diet high in saturated fats. cDNA isolated from livers from mice fed HFD, SO-HFD or Viv for 35 weeks, were 50bp pair-ended sequenced in triplicate using Illumina TruSeq RNA Sample Prep v2 Kit.
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Project description:Abstract Background In obesity, adipose tissue undergoes a remodeling process characterized by increased adipocyte size (hypertrophia) and number (hyperplasia). The individual ability to tip the balance toward the hyperplastic growth, with recruitment of new fat cells through adipogenesis, seems to be critical for a healthy adipose tissue expansion, as opposed to the development of inflammation and detrimental metabolic consequences. However, the molecular mechanisms underlying this fine-tuned regulation are far from being understood. Methods We analyzed by mass spectrometry-based proteomics visceral white adipose tissue (vWAT) samples collected from C57BL6 mice fed with a HFD for 8 weeks. A subset of these mice, called low responders (LowR HFD), showed a low susceptibility to the onset of adipose tissue inflammation, as opposed to their HFD counterpart. We identified the discriminants between LowR HFD and HFD vWAT samples and explored their function in Adipose Derived human Mesenchymal Stem Cells (AD-hMSCs) differentiated to adipocytes. Results We quantified 6051 proteins. Among the candidates that most differentiate LowR HFD from HFD vWAT, we found proteins involved in adipocyte function, including adiponectin and hormone sensitive lipase, suggesting that adipocyte differentiation is enhanced in LowR HFD, as compared to HFD. The chromatin modifier SET and MYND Domain Containing 3 (SMYD3), whose function in adipose tissue was totally unknown, was another top-scored hit. SMYD3 expression was significantly higher in LowR HFD vWAT, as confirmed by western blot analysis. In vitro, we found that SMYD3 mRNA and protein levels decrease rapidly along the differentiation process of AD-hMSCs. Moreover, SMYD3 knock-down at the beginning of adipocyte differentiation resulted in reduced cell proliferation and, at longer term, reduced lipid accumulation in adipocytes. Conclusions Our study describes for the first time the role of SMYD3 as a regulator of adipocyte proliferation during the early steps of adipogenesis.
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Project description:Chronic kidney disease (CKD) has emerged as a significant global public health issue due to its rising prevalence. The co-morbidity of CKD and diabetes is becoming increasingly severe, with diabetes being a primary cause of CKD leading to end-stage kidney disease (ESKD). Therefore, there is an urgent need to develop drugs that offer comprehensive benefits for patients with diabetes and CKD. This has also become a trend in the development of new hypoglycemic drugs. SZ-A is a natural drug approved by the National Medical Products Administration (NMPA) for treating type 2 diabetes mellitus. It has been shown to have good hypoglycemic effects and excellent safety. Subsequent in-depth studies have confirmed that it also has multiple pharmacological effects, including inhibiting colon inflammation, reducing body weight, alleviating non-alcoholic fatty liver disease, and improving insulin resistance. Our team's preliminary research found that SZ-A has the potential to significantly improve the progression of diabetic nephropathy and has a wide distribution in renal tissues. However, the mechanism by which SZ-A exerts its renoprotective effects has not been fully elucidated. It is unclear whether its effect on renal function is dependent on its glucose-lowering effect or if it acts directly on the kidney. The objective of this study was to evaluate the effect of SZ-A on non-diabetic chronic kidney disease by constructing an adenine-induced chronic kidney disease model. The study aimed to explore the mechanism of action of SZ-A in depth, both in vivo and ex vivo, and to elucidate the effect and mechanism of action of SZ-A and its components on renal function. The study results indicate that SZ-A can alleviate adenine-induced renal function decline in a dose-dependent manner. This therapeutic effect does not depend on the glucose-lowering effect. The SZ-A treatment group exhibited improvements in renal fibrosis, inflammation, and oxidative stress compared to the model group. Renal transcriptome analysis revealed that the protective effect of SZ-A was associated with enhanced fatty acid oxidation and decreased inflammation. Both the animal and cellular levels confirmed SZ-A's ameliorative effect on these factors, with DNJ playing a significant role. This study presents an innovative finding on the molecular mechanism through which SZ-A enhances renal function in patients with type 2 diabetes mellitus and concurrent CKD. The study reveals that SZ-A regulates energy metabolism, protects mitochondria, and identifies the single component that plays a major role. These findings provide scientific support for expanding therapeutic options and promoting the rationalization of drug use in clinical settings.
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